Effect of dimethyl sulfoxide on inhibition of post-ovariectomy osteopenia in rats

Tamjidipoor, Ahmad; Tavafi, Majid; Ahmadvand, Hasan

doi:10.3109/03008207.2013.841678

Cited by 4 publications

(5 citation statements)

References 48 publications

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“…We cannot exclude systemic inflammatory effects on bone healing, but – if present – they did not affect overall health (as seen by the analyses of body weight, food intake and general conditions [18]. DMSO itself in a high dose could ameliorate post-ovariectomy osteopenia [76], but all of our groups received the same amounts (even OVX and NON-OVX). Cortical width as it is measured in the sagittal plane (Fig.…”

Section: Limitationsmentioning

confidence: 99%

Effect of the lipoxygenase inhibitor baicalein on bone tissue and bone healing in ovariectomized rats

Saul¹,

Weber²,

Zimmermann³

et al. 2019

Nutr Metab (Lond)

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BackgroundOsteoporosis is one of the world’s major medical burdens in the twenty-first century. Pharmaceutical intervention currently focusses on decelerating bone loss, but phytochemicals such as baicalein, which is a lipoxygenase inhibitor, may rescue bone loss. Studies evaluating the effect of baicalein in vivo are rare.MethodsWe administered baicalein to sixty-one three-month-old female Sprague-Dawley rats. They were divided into five groups, four of which were ovariectomized (OVX) and one non-ovariectomized (NON-OVX). Eight weeks after ovariectomy, bilateral tibial osteotomy with plate osteosynthesis was performed and bone formation quantified. Baicalein was administered subcutaneously using three doses (C1: 1 mg/kg BW; C2: 10 mg/kg BW; and C3: 100 mg/kg BW) eight weeks after ovariectomy for four weeks. Finally, femora and tibiae were collected. Biomechanical tests, micro-CT, ashing, histological and gene expression analyses were performed.ResultsBiomechanical properties were unchanged in tibiae and reduced in femora. In tibiae, C1 treatment enhanced callus density and cortical width and decreased callus area. In the C3 group, callus formation was reduced during the first 3 weeks after osteotomy, correlating to a higher mRNA expression of Osteocalcin, Tartrate-resistant acid phosphatase and Rankl. In femora, baicalein treatments did not alter bone parameters.ConclusionsBaicalein enhanced callus density and cortical width but impaired early callus formation in tibiae. In femora, it diminished the biomechanical properties and calcium-to-phosphate ratio. Thus, it is not advisable to apply baicalein to treat early bone fractures. To determine the exact effects on bone healing, further studies in which baicalein treatments are started at different stages of healing are needed.Electronic supplementary materialThe online version of this article (10.1186/s12986-018-0327-2) contains supplementary material, which is available to authorized users.

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Section: Limitationsmentioning

confidence: 99%

Effect of the lipoxygenase inhibitor baicalein on bone tissue and bone healing in ovariectomized rats

Saul¹,

Weber²,

Zimmermann³

et al. 2019

Nutr Metab (Lond)

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“…Sahin et al reported that DMSO caused to decrease MDA levels in liver of IR injury-induced rabbits compared to untreated IR group rabbits [ 63 ]. Tamjidipoor et al showed MDA levels were increased after ovariectomy and decreased after DMSO application in rats [ 64 ]. Li et al indicated that Zymosan injection increased MDA levels and DMSO suppressed the increase of MDA in Zymosan-induced intestinal inflammation model in rats [ 65 ].…”

Section: ⧉ Discussionmentioning

confidence: 99%

Carvacrol treatment opens Kir6.2 ATP-dependent potassium channels and prevents apoptosis on rat testis following ischemia–reperfusion injury model

Balcı

Fırat²,

Acar³

et al. 2021

Rom J Morphol Embryol

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Testicular torsion is a urological problem that causes subfertility and testicular damage in males. Testis torsion and detorsion lead to ischemiareperfusion (IR) injury in the testis. Testicular IR injury causes the increase of reactive oxygen species (ROS), oxidative stress (OS) and germ cell-specific apoptosis. In this study, we aimed to investigate whether Carvacrol has a protective effect on testicular IR injury and its effects on Kir6.2 channels, which is a member of adenosine triphosphate (ATP)-dependent potassium channels. In the study, 2-4 months old 36 albino Wistar rats were used. For experimental testicular IR model, the left testis was rotated counterclockwise at 720º for two hours, and after two hours following torsion, detorsion was performed. Carvacrol was dissolved in 5% Dimethyl Sulfoxide (DMSO) at a dose of 73 mg/kg and half an hour before detorsion, 0.2 mL was administered intraperitoneally. In testicular tissues, caspase 3 and Kir6.2 immunoexpressions were examined. Serum malondialdehyde (MDA) and testosterone levels were measured. Apoptotic cells and serum MDA levels were significantly decreased and Kir6.2 activation was significantly increased in Carvacrol-administrated IR group. As a result of our study, Carvacrol may activates Kir6.2 channels and inhibits apoptosis and may have a protective effect on testicular IR injury.

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“…Further studies using osteoclast precursors of human origin are essential to determine the optimum concentration of DMSO for the inhibition of osteoclasts in therapeutic applications. A recent study utilizing ovariectomized rats demonstrated that intra-peritoneal injections of 0.5, 1 and 2 ml DMSO kg/day inhibited estrogen deficiency-induced osteopenia in these rats by inhibiting the function of the (Tamjidipoor et al 2013). DMSO given orally has a very low toxicity (LD50=14.5 g/kg body weight) in humans, and uncontrolled clinical trials that used topical application of DMSO for the treatment of a variety of musculoskeletal Fig.…”

Section: Discussionmentioning

confidence: 99%

“…A recent study revealed that the decrease in bone density associated with estrogen deficiency-induced oxidative stress was significantly inhibited by DMSO in ovariectomized rats (Tamjidipoor et al 2013). Importantly, DMSO protected post-ovariectomy bone loss through decreasing osteoclast numbers in the tibia (Tamjidipoor et al 2013). These reports suggest that further insights into the action of DMSO on cell types of the musculoskeletal system will be beneficial in determining the usefulness of DMSO for various applications.…”

Section: Introductionmentioning

confidence: 99%

“…Although several uncontrolled clinical studies have shown beneficial effects of DMSO in reducing osteoarthritis-related swelling, pain and in increasing motion in large cohorts (John and Laudahn 1967;Demos et al 1967;Rosenbaum et al 1965;Paul 1967;Lockie and Norcross 1967), a recent review of randomized controlled trials which used DMSO for the treatment of osteoarthritis concluded that no definitive conclusions can be drawn due to the mixed findings and the use of inadequate dosing periods (Brien et al 2011). A recent study revealed that the decrease in bone density associated with estrogen deficiency-induced oxidative stress was significantly inhibited by DMSO in ovariectomized rats (Tamjidipoor et al 2013). Importantly, DMSO protected post-ovariectomy bone loss through decreasing osteoclast numbers in the tibia (Tamjidipoor et al 2013).…”

Section: Introductionmentioning

confidence: 99%

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Inhibition of differentiation and function of osteoclasts by dimethyl sulfoxide (DMSO)

et al. 2015

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Dimethyl sulfoxide (DMSO) is an FDA-approved organosulfur solvent that is reported to have therapeutic value in osteoarthritis and osteopenia. DMSO is used as a cryoprotectant for the cryopreservation of bone grafts and mesenchymal stem cells which are later used for bone repair. It is also used as a solvent in the preparation of various scaffolds used for bone tissue engineering purposes. DMSO has been reported to inhibit osteoclast formation in vitro but the mechanism involved has remained elusive. We investigated the effect of DMSO on osteoclast differentiation and function using a conventional model system of RAW 264.7 cells. The differentiation of RAW 264.7 cells was induced by adding 50 ng/ml RANKL and the effect of DMSO (0.01 and 1% v/v) on RANKL-induced osteoclastogenesis was investigated. Addition of 1% DMSO significantly inhibited RANKL-induced formation of TRAP+, multinucleated, mature osteoclasts and osteoclast late-stage precursors (c-Kit(-) c-Fms(+) Mac-1(+) RANK(+)). While DMSO did not inhibit proliferation per se, it did inhibit the effect of RANKL on proliferation of RAW 264.7 cells. Key genes related to osteoclast function (TRAP, Integrin αVβ3, Cathepsin K and MMP9) were significantly down-regulated by DMSO. RANKL-induced expression of RANK gene was significantly reduced in the presence of DMSO. Our data, and reports from other investigators, that DMSO enhances osteoblastic differentiation of mesenchymal stem cells and also prevents bone loss in ovarietcomized rats, suggest that DMSO has tremendous potential in the treatment of osteoporosis and bone diseases arising from uncontrolled activities of the osteoclasts.

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Effect of dimethyl sulfoxide on inhibition of post-ovariectomy osteopenia in rats

Cited by 4 publications

References 48 publications

Effect of the lipoxygenase inhibitor baicalein on bone tissue and bone healing in ovariectomized rats

Effect of the lipoxygenase inhibitor baicalein on bone tissue and bone healing in ovariectomized rats

Carvacrol treatment opens Kir6.2 ATP-dependent potassium channels and prevents apoptosis on rat testis following ischemia–reperfusion injury model

Inhibition of differentiation and function of osteoclasts by dimethyl sulfoxide (DMSO)

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